Fig.18.11 wasrecordedfromaquadriplegicpatientwhocouldnotbreathespontaneouslyandrequiredtrachealintubationandartificialrespiration.Whenthetrachealcatheterwasbrieflydisconnected(nearthebeginningofthetopstripinthefigure,indicatedbythearrow)toallownursingcare,profoundbradycardiadevelopedafter9heartbeats.Thepatient’sheartratewas65beatsperminutejustbeforethetrachealcatheterwasdisconnected.Inlessthan10secondsaftercessationofartificialrespiration,hisheartratedroppedtoapproximately20beatsperminute.Thisbradycardiacouldbepreventedbyblockingtheeffectsofefferentvagalactivitywithatropine,anditsonsetcouldbedelayedconsiderablybyhyperventilationofthepatientbeforethetrachealcatheterisdisconnected.
by the arterial baroreceptors. Excitation of these endocardial receptors causes the heart rate and peripheral resistance to diminish. Other sensory receptors have been identified in the epicardial regions of the ventricles. Although all these ventricular receptors are excited by various mechanical and chemical stimuli, their exact physiological functions remain unclear.
Regulation of Myocardial Performance
Intrinsic Regulation of Myocardial Performance
As noted previously, the heart can initiate its own beat in the absence of any nervous or hormonal control. The myocardium can also adapt to changing hemodynamic conditions by means of mechanisms that are intrinsic to cardiac muscle itself. For example, racing greyhounds with •Fig. 18.11 Electrocardiogram of a 30-Year-Old Quadriplegic Man Who Could Not Breathe Spontaneously and Required Tracheal Intubation and Artificial Respiration. Thetwostripsarecontinuous.(ModifiedfromBerkJL,LevyMN.Eur Surg Res. 1977;9:75.) denervated hearts perform almost as well as those with intact innervation. Their maximal running speed decreases by only 5% after complete cardiac denervation. In these dogs, the threefold to fourfold increase in cardiac output during a race is achieved principally by an increase in stroke volume. Normally, the increase in cardiac output with exercise is accompanied by a proportionate increase in heart rate; stroke volume does not change much (see ). This adaptation in the denervated heart is not achieved entirely by intrinsic mechanisms; circulating catecholamines undoubtedly contribute. For example, if β-adrenergic receptor antagonists are given to greyhounds with denervated hearts, their racing performance is severely impaired.
Ventricularreceptorshavebeenimplicatedintheinitiationofvasovagal syncope, afeelingoflightheadednessorbrieflossofconsciousnessthatmaybetriggeredbypsychologicalororthostaticstress.Theventricularreceptorsarebelievedtobestimulatedbyreducedventricularfillingvolumeincombinationwithvigorousventricularcontraction.Inapersonstandingquietly,ventricularfillingisdiminishedbecausebloodtendstopoolintheveinsintheabdomenandlegs,asexplainedin
Chapter17.
Consequently,thereductionincardiacoutputandarterialbloodpressureleadstoageneralizedincreaseinsympatheticneuralactivitythroughthebaroreceptorreflex(see
Fig.18.5 ).Theenhancedsympatheticactivitytotheheartevokesavigorousventricularcontractionthatstimulatestheventricularreceptors.Excitationoftheventricularreceptorsinitiatestheautonomicneuralchangesthatevokevasovagalsyncope:namely,acombinationofprofound,vagallymediatedbradycardiaandgeneralizedarteriolarvasodilationmediatedbyareductioninsympatheticneuralactivity.